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Cancer Science & Therapy

Cancer Science & Therapy

ISSN: 1948-5956

Open Access

Short Communication - (2025) Volume 17, Issue 3

Hannah Robinson*
*Correspondence: Hannah Robinson, Department of Translational Cancer Research, University of Toronto, Toronto, ON M5S 1A1, Canada, Email:
1Department of Translational Cancer Research, University of Toronto, Toronto, ON M5S 1A1, Canada

Received: 01-May-2025 Editor assigned: 05-May-2025 Reviewed: 19-May-2025 Revised: 22-May-2025 Published: 29-May-2025 , DOI: 10.37421/1948-5956.2025.17.709
Citation: Hannah Robinson. ”Epigenetics in Cancer: Impact, Targets and Therapeutic Promise.” J Cancer Sci Ther 17 (2025):709.
Copyright: © 2025 R. Hannah This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Introduction

This article delves into how epigenetics, particularly DNA methylation, histone modification, and non-coding RNAs, controls cancer stem cell properties. It highlights the potential for targeting these epigenetic mechanisms to improve cancer therapies, suggesting new approaches for treating resistant tumors [1].

This review examines the current landscape of epigenetic therapies in cancer treatment, focusing on drugs targeting DNA methyltransferases and histone deacetylases. It discusses their mechanisms of action, clinical applications, and the challenges in developing more effective and specific epigenetic drugs, offering a glimpse into future directions [2].

This article explores the epigenetic modifications occurring within the tumor microenvironment (TME), which profoundly influence tumor progression and immune evasion. It identifies key epigenetic regulators in the TME as promising targets for novel cancer therapies, aiming to overcome resistance and enhance existing treatments [3].

This review explores the critical roles of various non-coding RNAs, like microRNAs and lncRNAs, in modulating epigenetic processes that drive cancer initiation and progression. It highlights their potential as innovative therapeutic targets and diagnostic biomarkers, paving the way for more precise cancer management [4].

This article surveys the promising field of epigenetic biomarkers, such as altered DNA methylation patterns and histone modifications, for the early detection and prognostic assessment of various cancers. It discusses their advantages over traditional markers and the challenges in their clinical translation, underscoring their potential to revolutionize cancer screening [5].

This paper investigates the intricate relationship between dietary factors and epigenetic modifications in cancer development and progression. It highlights how specific nutrients and dietary patterns can influence DNA methylation and histone acetylation, offering a fascinating avenue for cancer prevention and complementary therapeutic strategies [6].

The article explores the crucial role of histone modifications, such as acetylation, methylation, and phosphorylation, in shaping the cancer epigenome. It discusses how dysregulation of these modifications contributes to oncogenesis and highlights the development of targeted therapies that modulate these epigenetic marks, offering new therapeutic avenues [7].

This paper discusses the emerging field of epigenetic liquid biopsy, using circulating tumor DNA and other biofluids to detect cancer-specific epigenetic alterations. It underscores the potential of this non-invasive approach for early diagnosis, monitoring treatment response, and detecting recurrence, which is really game-changing [8].

This article explores the fascinating synergy between epigenetic modulation and cancer immunotherapy. It reveals how epigenetic drugs can reprogram the tumor microenvironment and enhance immune responses, making otherwise resistant tumors more susceptible to immunotherapy. This combined approach promises improved patient outcomes [9].

This paper investigates the intricate connection between altered cellular metabolism and epigenetic dysregulation in cancer cells. It illustrates how metabolic intermediates can act as cofactors for epigenetic enzymes, driving oncogenic changes, and suggests that targeting this metabolic-epigenetic crosstalk could open new avenues for cancer therapy [10].

Description

Epigenetics plays a fundamental and intricate role in the development and progression of cancer, with various mechanisms profoundly influencing cellular properties and disease characteristics. At a core level, mechanisms like DNA methylation, histone modification, and non-coding RNAs are recognized as crucial regulators of cancer stem cell properties. Understanding these regulatory pathways offers promising avenues for improving cancer therapies, particularly for treating resistant tumors [1]. Complementing this, the dysregulation of histone modifications, which include acetylation, methylation, and phosphorylation, significantly shapes the cancer epigenome. Such alterations are direct contributors to oncogenesis, highlighting the importance of developing targeted therapies that specifically modulate these epigenetic marks to open new therapeutic avenues [7].

The evolving therapeutic landscape in cancer treatment increasingly incorporates epigenetic approaches. Current strategies commonly involve drugs designed to target key enzymes such as DNA methyltransferases and histone deacetylases. While these drugs show promise, the development of more effective and specific epigenetic agents remains a significant challenge, guiding future research directions in oncology [2]. Beyond targeting individual cells, the tumor microenvironment (TME) is another critical area where epigenetic modifications occur. These changes profoundly influence tumor progression and contribute to immune evasion. Identifying and targeting key epigenetic regulators within the TME is therefore considered a promising strategy for novel cancer therapies, with the goal of overcoming treatment resistance and enhancing the efficacy of existing interventions [3].

Non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play critical roles in modulating the epigenetic processes that underpin both cancer initiation and progression. Their diverse functions position them not only as innovative therapeutic targets but also as valuable diagnostic biomarkers, holding the potential for more precise and personalized cancer management strategies [4]. In parallel, the field of epigenetic biomarkers is rapidly advancing, offering new tools for early detection and prognostic assessment. These biomarkers, which include altered DNA methylation patterns and specific histone modifications, offer distinct advantages over traditional markers. Despite challenges in their clinical translation, their potential to revolutionize cancer screening and improve patient outcomes is substantial [5].

External factors, such as dietary components, are increasingly recognized for their influence on epigenetic modifications relevant to cancer development and progression. Research highlights how specific nutrients and overall dietary patterns can impact crucial epigenetic processes like DNA methylation and histone acetylation. This presents fascinating avenues for cancer prevention and the integration of complementary therapeutic strategies [6]. Furthermore, there is a deep and intricate connection between altered cellular metabolism and epigenetic dysregulation in cancer cells. Metabolic intermediates often serve as cofactors for epigenetic enzymes, directly driving oncogenic changes. Targeting this complex metabolic-epigenetic crosstalk is emerging as a novel approach to develop new cancer therapies [10].

Advanced diagnostic and therapeutic strategies are continuously being developed to combat cancer more effectively. The emergence of epigenetic liquid biopsy is particularly noteworthy. This non-invasive method utilizes circulating tumor DNA and other biofluids to detect cancer-specific epigenetic alterations, offering immense potential for early diagnosis, real-time monitoring of treatment response, and detecting disease recurrence. This technology is truly game-changing for clinical practice [8]. Additionally, the fascinating synergy between epigenetic modulation and cancer immunotherapy is a burgeoning area of research. Epigenetic drugs have demonstrated the capacity to reprogram the tumor microenvironment and enhance immune responses. This makes otherwise resistant tumors more susceptible to immunotherapy, and this combined approach holds significant promise for dramatically improving patient outcomes in the future [9].

Conclusion

Epigenetics plays a central role in cancer development and progression, encompassing a range of mechanisms from DNA methylation and histone modifications to non-coding RNAs. These epigenetic processes control critical aspects like cancer stem cell properties, influence the tumor microenvironment, and drive oncogenesis. Current therapeutic approaches target epigenetic enzymes such as DNA methyltransferases and histone deacetylases, with ongoing efforts to develop more effective and specific drugs. Beyond therapies, the field is advancing with epigenetic biomarkers for early detection and prognosis, and the innovative use of epigenetic liquid biopsy for non-invasive diagnosis and monitoring. Research also highlights how external factors like diet and internal metabolic reprogramming interact with epigenetics, offering new avenues for cancer prevention and therapy. Furthermore, combining epigenetic modulation with immunotherapy shows promise in enhancing immune responses and overcoming treatment resistance, suggesting improved patient outcomes. This diverse exploration of epigenetics underscores its multifaceted impact and therapeutic potential in cancer.

Acknowledgement

None.

Conflict of Interest

None.

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